Linked Life Data

21345970

Source:http://linkedlifedata.com/resource/pubmed/id/21345970

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2011-6-1
pubmed:abstractText
IL-27, an IL-12 family member, was initially described as a proinflammatory cytokine. Nevertheless, it also poses anti-inflammatory activity, being involved in suppressing development of TH-17 cells as well as in the induction of inhibitory Tr1 cells. Recent data obtained in mice suggest that it can down-modulate the function of APCs. However, until now, nothing was known about the influence of IL-27 on human DCs. We investigated the effect of IL-27 on in vitro human MoDCs and on ex vivo blood DCs. Our results show that treatment of mDCs with IL-27 led to specific up-regulation of surface expression of several molecules, including B7-H1, in the absence of general DC maturation. Moreover, we demonstrated that IL-27-treated DCs exhibit a reduced capacity to stimulate proliferation and cytokine production of allogeneic T cells as compared with control DCs. Decisively, we identified B7-H1 as a crucial molecule, responsible for suppressive effects of "IL-27 DC" on T cells. Our data demonstrate for the first time that in addition to the dual role of IL-27 in the modulation of T cell activation and differentiation, human IL-27 modulates an immune response through DCs, i.e., by inducing immunosuppressive B7-H1 molecules and reducing the stimulatory potential of DCs.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
1938-3673
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
89
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
837-45
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed:year
2011
pubmed:articleTitle
IL-27 renders DC immunosuppressive by induction of B7-H1.
pubmed:affiliation
Department of Dermatology, University of Heidelberg, Im Neuenheimer Feld 350, Heidelberg, Germany. svetlana.karakhanova@med.uni-heidelberg.de
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't